SummaryPlasma oxytocin levels were measured serially in 22 women receiving prostaglandin E, or F2,: intravenously for the induction of labour. Oxytocin was detected in the plasma of 19 of the 22 women; positive levels were found in 60 (43/0o) of 139 plasma samples, an incidence similar to that in the late first stage of spontaneous labour. Oxytocin was found in the maternal plasma even when the fetus was dead, and in the plasma of two men receiving prostaglandin infusions. This indicates that prostaglandins stimulate the pituitary directly and suggests that this mechanism may play a part in the oxytocic action of infused prostaglandins. IntroductionThe prostaglandins produce many diverse actions indirectly by stimulating the hormone system specific to the organ concerned (Flack et al., 1969;Kaneko et al., 1969;Aldridge et al., 1970;Kuehl et al., 1970;Speroff and Ramwell, 1970;Marsh, 1971). We have investigated the possibility that the prostaglandins produce their effect on the uterus by releasing oxytocin from the maternal pituitary.

Summary The possibility that ketonic prostaglandins (PGEs) and oxytocin (Syntocinon, Sandoz) may be used to supplement each other on the pregnant human uterus has been investigated in vitro. The enhancement effect of E prostaglandins on the myometrial response to oxytocin is described both for mid‐trimester and term myometrial strips. An hypothesis regarding the role of prostaglandins in labour is put forward and discussed. The application of this sensitizing effect to the induction of mid‐trimester abortion is also considered.

SUMMARY The levels of prostaglandins E, A, and 19 hydroxy A in samples of seminal fluid collected from men attending a fertility clinic have been estimated spectrophotometrically and compared with levels found in samples from fertile men undergoing sterilization by vasectomy. Semen taken from oligo or aspermic men and that from men whose wives proved infertile did not contain significantly different amounts of prostaglandin from samples taken from fertile men. However, a smaller scatter of values for PGE content was found in the group where infertility was unexplained. This was significant (P<0.025). It was also found that considerable deterioration of samples occurred on storage.

Summary Interaction between prostaglandins and Syntocinon is shown to be of two kinds. There may be potentiation, where an increased response to Syntocinon follows combination with a low dose of prostaglandin, and enhancement, which is of much longer duration. Potentiation can be produced by both E and F prostaglandins, whereas enhancement is confined to E prostaglandins. Varying the doses of prostaglandin E is shown to have little effect on the degree of enhancement produced. The physiological implications and clinical applications of these interactions are discussed.

This paper describes an easy and relatively rapid procedure for distinguishing the ketonic prostaglandins E (PGEs) from the non-ketonic prostaglandins F (PGFs) and other hydroxy-acid lipid spasmogens. The method depends on the ability of certain hydrazine derivatives to combine specifically with keto groups. The condensation reaction leads to the formation of hydrazones according to the equation: RR'CO + H2N.NHR". 'RR'C=N.NHR" + H2OTo obtain this ketonic condensation we have used Girard's reagent T (trimethylammonium-acetohydrazide chloride, H2N.NH.CO.CH2.N(CH3)3C1), which is one of a series of reagents developed by Girard & Sandulesco (1936); these reagents are soluble in water and insoluble in non-hydroxylated organic solvents. The hydrazones formed from ketones and reagent T are also more water and less ether-soluble than the original ketones. In preliminary trials with known compounds it was found that treatment of ketonic PGEs in aqueous solution with reagent T leads, as expected, to an apparent retention of the product in the water phase during subsequent partitions with diethyl ether at pH 3-4; this reduced extractability of PGEs will be referred to as an apparent inactivation. On the other hand, the non-ketonic PGFs were recovered fully from the ether phase, indicating absence of reaction with the reagent, as expected from the difference in its structure at C9, which is shown above.Reagent T is itself insoluble in ether and did not interfere with the assays of prostaglandins.The reduction in ether-extractability of PGEs by reagent T was applied for the detection of prostaglandin-like spasmogenic keto-hydroxy-acids previously found in this laboratory in